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Redox Balance, Antioxidant Defense, and Oxidative Damage in the Hypothalamus and Cerebral Cortex of Rats with High Fat Diet-Induced Insulin Resistance
المؤلفون المشاركون
Maciejczyk, M.
Zalewska, A.
Żebrowska, Ewa
Chabowski, Adrian
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-09-06
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
Oxidative stress is a key pathogenic factor in both neurogenerative and metabolic diseases.
However, its contribution in the brain complications of insulin resistance is still not well understood.
Therefore, the aim of this study was the evaluation of redox homeostasis and oxidative damage in the hypothalamus and cerebral cortex of insulin-resistant and control rats.
16 male Wistar rats were divided into two equal groups (n=8): the control and high fat diet group (HFD).
Prooxidant enzymes (xanthine oxidase and NADPH oxidase); enzymatic and nonenzymatic antioxidants [glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), superoxide dismutase-1 (SOD-1), and uric acid (UA)]; and oxidative damage products [advanced glycation end products (AGE), 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG)] as well as the total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), and total ferric reducing ability of sample (FRAP) were evaluated in the hypothalamus and cerebral cortex as well as serum/plasma of HFD-fed and control rats.
The activity of prooxidant enzymes was significantly increased in the cerebral cortex and hypothalamus of HFD-fed rats vs.
control rats.
Additionally, we have showed enhanced antioxidant efficiency in the hypothalamus (↑CAT, ↑UA, ↑TAC, and ↑FRAP) and cerebral cortex (↑GPx, ↑CAT, ↑SOD-1, ↑UA, ↑TAC, and ↑FRAP) of HFD-fed rats.
All of the oxidative damage markers (AGE, 4-HNE, MDA, 8-OHdG, and OSI) were significantly increased in the cerebral cortex of insulin-resistant rats, while only 4-HNE and MDA were markedly higher in the hypothalamus of the HFD group.
Summarizing, the results of our study indicate an adaptive brain response to the increased production of free radicals under insulin resistance conditions.
Despite the increase in antioxidative defense systems, this mechanism does not protect both brain structures from oxidative damages.
However, the cerebral cortex is more susceptible to oxidative stress caused by HFD.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Maciejczyk, M.& Żebrowska, Ewa& Zalewska, A.& Chabowski, Adrian. 2018. Redox Balance, Antioxidant Defense, and Oxidative Damage in the Hypothalamus and Cerebral Cortex of Rats with High Fat Diet-Induced Insulin Resistance. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-11.
https://search.emarefa.net/detail/BIM-1211889
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Maciejczyk, M.…[et al.]. Redox Balance, Antioxidant Defense, and Oxidative Damage in the Hypothalamus and Cerebral Cortex of Rats with High Fat Diet-Induced Insulin Resistance. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-11.
https://search.emarefa.net/detail/BIM-1211889
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Maciejczyk, M.& Żebrowska, Ewa& Zalewska, A.& Chabowski, Adrian. Redox Balance, Antioxidant Defense, and Oxidative Damage in the Hypothalamus and Cerebral Cortex of Rats with High Fat Diet-Induced Insulin Resistance. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-11.
https://search.emarefa.net/detail/BIM-1211889
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1211889
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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